CA916798 gene participates in cisplatin resistance of human lung adenocarcinoma A549 cells through PI3K/AKT/mTOR pathway.
- Author:
Zhanzhong QI
1
;
Yuliang WANG
;
Xiangdong ZHOU
Author Information
- Publication Type:Journal Article
- MeSH: Cell Line, Tumor; Cell Proliferation; Cisplatin; pharmacology; Drug Resistance, Neoplasm; genetics; Humans; Phosphatidylinositol 3-Kinases; metabolism; Proto-Oncogene Proteins c-akt; metabolism; TOR Serine-Threonine Kinases; metabolism
- From: Journal of Southern Medical University 2012;32(9):1290-1293
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the changes of CA916798 gene expression in human lung adenocarcinoma cell A549 and the multidrug-resistant cell line A549/CDDP after blocking the PI3K/AKT/mTOR pathway.
METHODSHuman lung adenocarcinoma cell lines A549 and A549/CDDP were treated with rapamycin and LY294002, and the cell growth changes in response to subsequent cisplatin treatment was observed; RT-PCR was performed to detect CA916798 mRNA expression in the treated cells.
RESULTSBlocking PI3K/AKT/mTOR pathway with rapamycin and LY294002 significantly reduced drug resistance of both A549 and A549/CDDP cells to cisplatin and obviously decreased the expression of CA916798 gene mRNA (P<0.05).
CONCLUSIONCA9167981 gene is located downstream of the PI3K/AKT/mTOR pathway, which might be one of the mechanisms of CA916798 to cause cisplatin resistance in the tumor cells.